• Quick note - the problem with Youtube videos not embedding on the forum appears to have been fixed, thanks to ZiprHead. If you do still see problems let me know.

Real Cancer Cure Miracle

Now, to argue the other side of the coin, which is the obvious thing, if you do a medical procedure, a lot of times you do know that what you did worked. Because you did this, and this happened. If you did nothing, most likely it wouldn't have happened.

Surgery and other related procedures are the most obvious. Giving saline, heat, cold, cleaning a wound, many practical things have never been tested, as in double blind/placebo controlled studies, with large groups of people. Such testing is not required for many things.

But sometimes, as in the case of a few surgeries, such testing does show the procedure is useless, or worse, a dangerous and expensive procedure that does nothing.

It is, without a doubt, one of those things that can divide people. Where do you draw the line?

I can only speak for myself, but I still find it amazing when the 1000's of lines of hardware/software code I write result in the desired functionality.
 
You still haven't figured it out, robinson. You don't even know how much you don't know.

Let me put it another way. There is a large body of medical research that is in an entirely different ballpark than randomized clinical trials.

If I have more time, maybe I'll try to introduce you to some of it, for the sake of other readers anyway.
 
You don't need a control group to see a hammer was the cause of breaking a window if you observed the act.

That is exactly the reasoning used by many people, including scientist and researchers. And many who are labeled quacks, woo or other names. By employing a double standard, "skeptics" appear to be ignoring science they don't agree with, and supporting science they believe in. You can't logically use two different sets of rules when analyzing medical procedures. Either you rule out chance, placebo effect, bias and other factors, or you don't. To stand up, it must be replicated, tested, repeated and controlled.

Remission of cancer is a well known fact. Chance alone would mean there is the possibility of somebody having a "miracle" cure from cancer. In this specific case, I doubt that it was chance, but that is exactly why research uses methods that take the "belief" factor out of an experiment. It is all too easy to fool oneself.

What does it even mean? That the patient's tumors regressed spontaneously and it was just a coincidence?

Oddly enough, that is exactly the reasoning used to dismiss some results of studies. Research that does not use a control group can be dismissed, because it might be chance. Even when everybody in the study got better, it can be dismissed as "chance" if there is no control group. Or it is too small a sample.

You haven't even made the slightest attempt to see why your comment was so absurd.

Quite the contrary, you are the one that has gone quiet, and rather than support your case, you mistake insults for knowledge.

There is a large body of medical research that is in an entirely different ballpark than randomized clinical trials.

Indeed. And much of it considered woo woo, because it does not stand up to the level of evidence required to rule out factors and considerations that science requires. Even surgery and other procedures, once they are subjected to clinical trials, including sham surgery, (placebo), find that there is no benefit to something that "everybody knew worked".

If I have more time, maybe I'll try to introduce you to some of it, for the sake of other readers anyway.
:bs:

I noticed you have made 70 post in the Circumcision thread alone here, in the last week. You also have made 102 other posts, in the last week. 569 in the last month. Are you really that pressed for time?
 
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So what if I spent time on the forum and didn't address your lack of understanding of this research, rob. I don't owe you an education.
 
And now that I am back from my walk, I should also point out that I leave the computer on when I go out sometimes because I have a lot of stuff I am in th middle of that can be better to just leave on than to save and open later. I 'tab browse' so I stay logged on to the forum but I am often on another web site or I am writing some policies or doing other work on WORD. In Firefox you can have a dozen web sites open at the same time. For those of us impatient types it means I can do something else when a page is opening too slowly. Something this board is notorious for doing on occasion.
 
So let's get to this problem since you are probably unduly influencing people who don't understand what I am talking about and who may not be familiar with your typical posts.

That is exactly the reasoning used by many people, including scientist and researchers. And many who are labeled quacks, woo or other names. By employing a double standard, "skeptics" appear to be ignoring science they don't agree with, and supporting science they believe in. You can't logically use two different sets of rules when analyzing medical procedures. Either you rule out chance, placebo effect, bias and other factors, or you don't. To stand up, it must be replicated, tested, repeated and controlled.

Remission of cancer is a well known fact. Chance alone would mean there is the possibility of somebody having a "miracle" cure from cancer. In this specific case, I doubt that it was chance, but that is exactly why research uses methods that take the "belief" factor out of an experiment. It is all too easy to fool oneself.
If these scientists were merely infusing T cells into this patient and then waiting for a response, you would be describing the kind of research your reasoning is applicable to.

What makes that charge so ludicrous is that is far from how this research works.

Oddly enough, that is exactly the reasoning used to dismiss some results of studies. Research that does not use a control group can be dismissed, because it might be chance. Even when everybody in the study got better, it can be dismissed as "chance" if there is no control group. Or it is too small a sample.
No, the sample isn't too small. These researchers are not testing substances with trial and error. Trial and error does still have its place in research. And once a therapy is devised one must test it on a large number of patients to detect how all the individual differences in our genetic makeup are going to react to a treatment.

What you don't seem to realize is just how sophisticated and how specific molecular testing such as this has progressed. Just a few decades ago we were scouring the planet for all sorts of new substances that might have useful properties. This seek and test approach still goes on.

But the more advanced researchers are well beyond that. These guys are looking directly at the proteins and enzymes and neurotransmitters and codons. They are looking directly at the cancer cells in this case. They have detected what makes the cells divide, what makes them spread to distant sites, what stimulates the blood supply to grow to feed the cells, what shuts the cells down, and in this case, what attracts the immune response, what blocks it, and how the immune response destroys the cells and why the immune response loses the battle.

These guys are not just giving a treatment and looking for tumor regression. They designed the immune cells, multiplied them and directly observed them destroy the tumors. Like I said, if you watch the hammer break the window, you don't need a control to know the hammer broke the window. You just need to know that it has already been shown a hammer smashing against a window and a breaking window represent cause and effect.

And that is what we do know. We know how a Tcell destroys a cancer cell. So when we see a Tcell destroy a cancer cell we know it isn't a coincidence.

Quite the contrary, you are the one that has gone quiet, and rather than support your case, you mistake insults for knowledge.
I take it you are referring here to your insults about not seeing a control group in this research? If I didn't know you better, I'd be a bit more patient, assume maybe you were a teenager or something. But I know you too well. You have this odd belief that you have expertise which you don't really have. If you knew very much about molecular research of this kind, you'd recognize how little you really know.

Indeed. And much of it considered woo woo, because it does not stand up to the level of evidence required to rule out factors and considerations that science requires. Even surgery and other procedures, once they are subjected to clinical trials, including sham surgery, (placebo), find that there is no benefit to something that "everybody knew worked".
:dig:

You are digging your hole deeper and deeper as you are so confident in your limited knowledge that you haven't the sense to ask yourself, what might skeptigirl be talking about. I find myself questioned on occasion and it gives me enough pause to check out what it is I may be missing before digging that hole any deeper. It amazes me you have not even contemplated maybe there is something here you don't know. Mind boggling.

Ask yourself, robinson, if you understand what the following research papers are describing:

Lymphotactin Expression by Engineered Myeloma Cells Drives Tumor Regression: Mediation by CD41 and CD81 T Cells and Neutrophils Expressing XCR1 Receptor1

Cancer Regression and Autoimmunity in Patients After Clonal Repopulation with Antitumor Lymphocytes

Recombinant IL-12 administration induces tumor regression in association with IFN-gamma production

Regression of a Murine Gammaherpesvirus 68-Positive B-Cell Lymphoma Mediated by CD4 T Lymphocytes

Erythropoietin induces tumor regression and antitumor immune responses in murine myeloma models

Cellular Interactions in Effector Cell Generation and Tumor Regression Mediated by Anti-CD3/Interleukin 2-activated Tumor-draining Lymph Node Cells1

Tumor Regression and Autoimmunity after Reversal of a Functionally Tolerant State of Self-reactive CD8+ T Cells

Correlation between tumor regression and T cell responses in melanoma patients vaccinated with a MAGE antigen

CD4+CD25+ regulatory T cells that secrete TGFβ and IL-10 are preferentially induced by a vaccine vector

Macrophage-derived chemokine gene transfer results in tumor regression in murine lung carcinoma model through efficient induction of antitumor immunity

Autoimmunity Correlates With Tumor Regression in Patients With Metastatic Melanoma Treated With Anti–Cytotoxic T-Lymphocyte Antigen-4


Do you really think you are playing in this league?
 
When you get the time, here are some of the points waiting to be responded to. Well, you responded with some insults, but I mean scientific, logical type responses.

That is exactly the reasoning used by people putting DCA on skin cancer, then concluding that after 10 days has passed, when the cancer is gone, that the DCA caused the cancer cells to die. They even take photos of the entire event. Big Cancer on skin, then no cancer.

Yet that "Miracle" is dismissed by "authorities" as wishful thinking, bad science, or spontaneous remission.
Why is that? When you spend hundreds of thousands of dollars cloning and injecting cells, and one person out a hundred gets better, it is a miracle. But hundreds of people getting better, it needs more studies, more controls, it is flawed, it wasn't done with a placebo, we don't know if they would have gotten better anyway, it needs to be reproduced in large scale trials, yadda yadda yadda.

Same is true for a number of other "alternative" treatments for all kinds of medical issues. Unless it has large, repeatable studies, double blind placebo studies, anything can be dismissed.

To understand this, just imagine somebody started a thread about the Miracle of DCA, claiming it has been observed to halt or reverse tumor growth in hundreds of people. But with no study to back the claim up.

I know, that is a tough point to respond to.

There level of "evidence" is exactly the same as what this thread offers. Well, actually much higher, since the number of people is much greater.

In case it isn't perfectly clear, if a substance is KNOWN without a doubt to cause cancer to die, in animals, and in vivo, and then you add that one substance to a persons cancer, and the cancer starts dieing, some people think it is like throwing a hammer through a window. It is obvious.

Since cancer, Aids, and a host of other diseases are a result of the immune system not working right, why not boost the immune system, rather than treat the disease?

In this case, one could actually say, "We boosted his immune system, and the cancer is gone." And it doesn't sound woo!

Again, I think this sort of medical research is exactly what certain diseases need. This is possibly the real Orthomolecular medicine. Using the exact molecules to cure an exact condition.

Many of the case studies on DCA are done under the supervision and care of an oncologist. Almost all of them in fact. Because DCA is a very safe molecule, and can't hurt you, (if used correctly), adding it to current cancer treatments is done with the knowledge of the treating Physician.
Which is what makes this so interesting. Skeptigirl wants us to say, "if you throw a hammer through a window" you don't need blinding, controls, peer review, repeatability, all that scientific stuff.

I hope you didn't miss where I agreed with you. I'm pragmatic about most things. If it works, it can be obvious. In this case, it just isn't that simple however.

Because you did this, and this happened. Which is exactly the same reasoning many alternative therapies and treatments use. You don't need double blind/placebo controlled large scale studies to know something works. You do it, and you see what happens. End of story.

Several years ago another study was done, almost the same method, which used 19 patients, (none of whom survived, but one showed a small improvement), which was published. Not publishing your results in work like this is almost criminal, in regards to advancing science. It wasn't the same researchers who did the previous study. People build off of each others work.

The bugaboo of modern research, if you agree with it, you don't ask for anything else. If you don't agree, you demand repeated trials, vast amounts of precision, placebos, double blinding, huge numbers, and even then, when the results go against your preconceived ideas, you look for flaws in the study. Or simply say it wasn't enough.

In this case, what were the controls? Did all the people in the study have the same level of care? Same chemo going on? Diet? Exposure to sunlight? Radiation? Pollution? Genetics? Time with the cancer. Family history? Past history of cancer. Other diseases. Age? Sex?

Eliminating everything but the one thing you want to test, is very hard to do. In this case, how do we know that it was done?

Failures are just as important as succeeding in science. We learn what not to do.

I have heard of many cases where something stimulated the persons immune system, and they got rid of incurable cancers. There are many cases of that happening.

Which is why, one person does not make for a miracle. Those happen with regularity.

Knowing a Doctor is injecting you with a miracle, probably would have a powerful placebo effect. It could even trigger an immune response, even if it wasn't anything but saline. Which is why we do double blind/placebo controlled studies, to know what is really happening, side effects, dangers, etc etc yadda yadda yadda.

What I find hilarious, is that the people who insist that you can't know if something works, unless you jump through all those hoops, are now embracing this, as if it is a miracle. Except Dr. Imago, who seems most wise.

One case does not prove anything.

If you accept the same level of evidence in other cases, as in this case, there are hundreds of things that work. That have no evidence other than, "we did this, and this happened. It is a miracle!".

Okay. I can't argue with you here. It doesn't prove anything. It only points in what might be a promising direction. And I still think miracle is a good word for it. Why not? Spontaneous remission of any sort is often termed a miracle.

That is why I consider it research and science, not anything paranormal. There have been hundreds of other studies, lots of research that led up to this one success.

By employing a double standard, "skeptics" appear to be ignoring science they don't agree with, and supporting science they believe in. You can't logically use two different sets of rules when analyzing medical procedures. Either you rule out chance, placebo effect, bias and other factors, or you don't. To stand up, it must be replicated, tested, repeated and controlled.

Remission of cancer is a well known fact. Chance alone would mean there is the possibility of somebody having a "miracle" cure from cancer. In this specific case, I doubt that it was chance, but that is exactly why research uses methods that take the "belief" factor out of an experiment. It is all too easy to fool oneself.

Oddly enough, that is exactly the reasoning used to dismiss some results of studies. Research that does not use a control group can be dismissed, because it might be chance. Even when everybody in the study got better, it can be dismissed as "chance" if there is no control group. Or it is too small a sample.

Indeed. And much of it considered woo woo, because it does not stand up to the level of evidence required to rule out factors and considerations that science requires. Even surgery and other procedures, once they are subjected to clinical trials, including sham surgery, (placebo), find that there is no benefit to something that "everybody knew worked".


I hope you can enlighten us, and show why you consider some of that so insulting. Posting a list of papers isn't going to do it.
 
Robinson's comment underscored his ignorance of what this study was even about. And you want to join him?

Skeptigirl,

You don't need to lecture me about clinical trials. Trust me. Before I became a physician, I worked extensively in the clinical research arena, and I am familiar with all kinds of research, methodologies, protocol design, etc. from bench work to large, Phase III trials. I'm probably as, if not more, qualified than most on this forum to render an opinion.

I'm also familiar with the unique breeds of esoterica in basic research. Every department has one that can apply theory to limited applicability. We even have our own special group within my department that has received NIH funding to look at potential homology/heterogeneity in the mu-opioid receptor. They've produced a lot of interesting papers, but putting theory into practice is a different beast altogether.

Furthermore, I form my own opinions. I'm not "joining" anyone. If my opinions happen to align, even marginally, with someone else's, then call that coincidence. Nothing more.

What I do know is that modifying the immune system to battle cancer is not a new idea. It goes back decades. In small studies, investigators love to parade their successes. Where the rubber meets the road is the broad applicability of those successes, and whether or not the results can be reproduced, expanded, and then applied to a broad population. Cost and technical feasibility play into that ultimately before a "new" treatment modality can be considered a success.

Until such a time that another lab can take these successes (however minimal) and use this technology to effect a definitive cure in a similar patient population, you have to consider this research as nothing more than interesting speculation. Fact is, we don't know all the variables, this early in the 21st century, in tumorgenesis and regression. Additionally, the scientific literature is rife with so-called "miracle" cures in small patient subsets. I even worked on a compound when I was in the biotech industry that touted such successes in small groups of patients with malignant pleural effusion. When trials were expanded, the compound was subsequently abandoned because early successes did not mete larger ones.

I understand that there are small groups of investigators working in individual labs who can generate remissions in tough to treat and deadly diseases. This is important small-scale research that, at the very least, gives us greater insight into the mechanistic forces at play in certain cancers. However, what is still paramount is the ability to take these observations and successes, and reproduce them in other labs/clinics. Until that is done, the best you can call these observations is "promising".

As I stated before (numerous times), the proof is in the broad applicablility of such technologies - not the solo successes at one clinic. If this technology results in a high cure rate, is easy to reproduce at other institutions, and does not represent a cost-prohibitive solution, it will be adopted. It is interesting research that bears more investigation. But, I learned long ago not to get excited about such findings until they are independently verified.

If you want to call that "siding with Robinson", then that only demonstrates your limited comprehension of my cautious discernment of the findings and long history of involvement in similar research with hopes dashed on such seemingly promising results.

~Dr. Imago
 
Skeptigirl,

You don't need to lecture me about clinical trials. Trust me.... [snipped for convenience] ...
~Dr. Imago
Frankly, knowing you are a doc and assuming you understood the research, I was taken aback that you didn't recognize robinson's invalid critique that he didn't believe this research because there was no control group. Perhaps you had other issues and believed erroneously robinson was echoing those other issues.

Here is robinson's initial claim (emphasis mine):
[from the OP study] We show that the transferred CD4+ T cells mediated a durable clinical remission and led to endogenous responses against melanoma antigens other than NY-ESO-1.
As with Woo claims and treatments, without double blind placebo trials, they don't know that is the case at all. Especially considering the wealth of cases where similar situations occurred, after all hope was lost, and it was labeled, "spontaneous remission".

Where are the controls? What was the placebo? How large was he sample size? While some seem adverse to holding established medical authorities to a different standard, extraordinary claims require extraordinary evidence. Calling something a miracle doesn't change that.... Cmon skeptics, use your minds....
Note that I facetiously used the word "miracle" in the title to compare an evidence based cure with the claims of miracle cures.

You replied to the thread saying:
...My concern is that, even if ulitmately proven successful (noting Robinson's concerns), the broad applicability of such therapies will be cost prohibitive.

-Dr. Imago
What did you mean here by, "(noting Robinson's concerns)"? Did you mean you agree with robinson's premise that the researchers merely infused some cells, one patient was cured, and they are guessing their work directly resulted in this patient's tumor regression? Are you also claiming the result was guesswork and nothing more? Or did you mistakenly think robinson was making a sophisticated observation that it is premature to assume this research will eventually bear fruit?

Of course it is premature to conclude this research will ultimately be successful.
Neither the researchers nor I have said any such thing. I believe the entire field of research will ultimately be successful. But there is no way to predict what will come of this step along the way.

I went back over robinson's posts to be sure I was correctly reading that he thought the fact this wasn't a RCT made the research no more than guesswork. I find it incredulous that is what you were agreeing with.

(Again, emphasis mine.)
... leads terminal cases to try anything, even if it is woo as can be. What have they got to lose?

In an ironic sort of way, many people with cancer have already reported "cures" from DCA. There[sic] scientific method is pretty much the same as the one in the OP. "We did this, and a few people who did it, there[sic] cancer went away." Of course the same problem exists with there[sic] stories as the "Miracle" noted here. No controls, no double blind, and a very small group....
That is exactly the reasoning used by people putting DCA on skin cancer, then concluding that after 10 days has passed, when the cancer is gone, that the DCA caused the cancer cells to die. They even take photos of the entire event. Big Cancer on skin, then no cancer.

Yet that "Miracle" is dismissed by "authorities" as wishful thinking, bad science, or spontaneous remission.

Same is true for a number of other "alternative" treatments for all kinds of medical issues. Unless it has large, repeatable studies, double blind placebo studies, anything can be dismissed.

To understand this, just imagine somebody started a thread about the Miracle of DCA, claiming it has been observed to halt or reverse tumor growth in hundreds of people. But with no study to back the claim up.

There[sic] level of "evidence" is exactly the same as what this thread offers. Well, actually much higher, since the number of people is much greater.



So tell me, Dr Imago, do you think robinson is just saying that the research is preliminary, which no one is denying, or are you really agreeing with robinson that this specific research conclusion regarding this specific patient's response is a fraud?
 
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Now in regards to the rest of your comments...
...Before I became a physician, I worked extensively in the clinical research arena, and I am familiar with all kinds of research, methodologies, protocol design, etc. from bench work to large, Phase III trials. I'm probably as, if not more, qualified than most on this forum to render an opinion.

I'm also familiar with the unique breeds of esoterica in basic research. Every department has one that can apply theory to limited applicability. We even have our own special group within my department that has received NIH funding to look at potential homology/heterogeneity in the mu-opioid receptor. They've produced a lot of interesting papers, but putting theory into practice is a different beast altogether.

Furthermore, I form my own opinions. I'm not "joining" anyone. If my opinions happen to align, even marginally, with someone else's, then call that coincidence. Nothing more.

What I do know is that modifying the immune system to battle cancer is not a new idea. It goes back decades. In small studies, investigators love to parade their successes. Where the rubber meets the road is the broad applicability of those successes, and whether or not the results can be reproduced, expanded, and then applied to a broad population. Cost and technical feasibility play into that ultimately before a "new" treatment modality can be considered a success.
Where did you get the idea I disagree with any of this?

Until such a time that another lab can take these successes (however minimal) and use this technology to effect a definitive cure in a similar patient population, you have to consider this research as nothing more than interesting speculation. Fact is, we don't know all the variables, this early in the 21st century, in tumorgenesis and regression. Additionally, the scientific literature is rife with so-called "miracle" cures in small patient subsets. I even worked on a compound when I was in the biotech industry that touted such successes in small groups of patients with malignant pleural effusion. When trials were expanded, the compound was subsequently abandoned because early successes did not mete larger ones.

I understand that there are small groups of investigators working in individual labs who can generate remissions in tough to treat and deadly diseases. This is important small-scale research that, at the very least, gives us greater insight into the mechanistic forces at play in certain cancers. However, what is still paramount is the ability to take these observations and successes, and reproduce them in other labs/clinics. Until that is done, the best you can call these observations is "promising".

As I stated before (numerous times), the proof is in the broad applicablility of such technologies - not the solo successes at one clinic. If this technology results in a high cure rate, is easy to reproduce at other institutions, and does not represent a cost-prohibitive solution, it will be adopted. It is interesting research that bears more investigation. But, I learned long ago not to get excited about such findings until they are independently verified.
You really think I disagree with any of this? I think you need to reread the posts here because your reaction is one of someone who has grave misunderstanding of what has been posted.

If you want to call that "siding with Robinson", then that only demonstrates your limited comprehension of my cautious discernment of the findings and long history of involvement in similar research with hopes dashed on such seemingly promising results.

~Dr. Imago
No, it isn't siding with robinson at all. That is your problem. You appear to have skimmed the thread and jumped to a number of false conclusions about what both I and robinson posted.
 
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When you get the time, here are some of the points waiting to be responded to. Well, you responded with some insults, but I mean scientific, logical type responses.


Why is that? When you spend hundreds of thousands of dollars cloning and injecting cells, and one person out a hundred gets better, it is a miracle. But hundreds of people getting better, it needs more studies, more controls, it is flawed, it wasn't done with a placebo, we don't know if they would have gotten better anyway, it needs to be reproduced in large scale trials, yadda yadda yadda.
I used the word, miracle, facetiously.

Here's a bit more on what you don't seem to understand. To track the molecular response such as was done in this case is very expensive. Research at this stage is done well before any treatment is eventually developed that will then be tried in large RCTs.

When research on a treatment reaches the stage where it is actually ready for a large RCT, one cannot do these kinds of intensive molecular studies. It is possible to take random biopsies and test levels of specific T cells or test other immune responses. But RCTs are a long way off. You do not start with RCTs and as I said, we rarely still just try drugs out in a trial and error methodology. One starts with the direct interventions at the molecular level such as was done in this research.


I know, that is a tough point to respond to.
No, it isn't tough at all. I just explained it above.


In case it isn't perfectly clear, if a substance is KNOWN without a doubt to cause cancer to die, in animals, and in vivo, and then you add that one substance to a persons cancer, and the cancer starts dieing, some people think it is like throwing a hammer through a window. It is obvious.
I posted that list of studies for a reason, robinson. Obviously you didn't bother to look at them to get an idea at what level the research here is being conducted. Before I waste any more time, you need to look at the level sophistication in those studies. Look at what is being tested and observed. It isn't just a matter of applying a drug and doing an MRI to view the tumor. Your level of understanding here is lacking so much you have this grossly oversimplified view of what is being done here and because of it, you don't get why these researchers know this treatment worked in this patient.


Again, I think this sort of medical research is exactly what certain diseases need. This is possibly the real Orthomolecular medicine. Using the exact molecules to cure an exact condition.
Right concept, wrong claims by the people who use this terminology to make fake claims. It's like claiming homeopathy gives one chemical cures.

It is one thing to make some claim that every individual needs an individual vitamin regimen or whatever, and quite another to actually study the genetic and molecular mechanisms involved in tumor growth and immune system interaction with tumors of specific cancer types.


I hope you didn't miss where I agreed with you. I'm pragmatic about most things. If it works, it can be obvious. In this case, it just isn't that simple however.
Yes, it is that simple in this case. Whether it can be determined why this patient's treatment was successful when the other 8 patients' treatments were not and develop a useful treatment from this line of inquiry is another matter.


The bugaboo of modern research, if you agree with it, you don't ask for anything else. If you don't agree, you demand repeated trials, vast amounts of precision, placebos, double blinding, huge numbers, and even then, when the results go against your preconceived ideas, you look for flaws in the study. Or simply say it wasn't enough.

In this case, what were the controls? Did all the people in the study have the same level of care? Same chemo going on? Diet? Exposure to sunlight? Radiation? Pollution? Genetics? Time with the cancer. Family history? Past history of cancer. Other diseases. Age? Sex?

Eliminating everything but the one thing you want to test, is very hard to do. In this case, how do we know that it was done?
You are just repeating yourself here. See my previous response.


..I hope you can enlighten us, and show why you consider some of that so insulting. Posting a list of papers isn't going to do it.
Apparently not since you didn't get the point at all of the list of papers.


You are a perfect example, as I said, of someone who doesn't understand they are drawing false conclusions because they don't know what it is they don't know.
 
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That is exactly the reasoning used by many people, including scientist and researchers. And many who are labeled quacks, woo or other names. By employing a double standard, "skeptics" appear to be ignoring science they don't agree with, and supporting science they believe in. You can't logically use two different sets of rules when analyzing medical procedures. Either you rule out chance, placebo effect, bias and other factors, or you don't. To stand up, it must be replicated, tested, repeated and controlled.

Robinson, one reason why I find this sort of research more convincing than typical anecdotal evidence is that they know exactly how many people they attempted this treatment on. In the case of bee stings and other anecdotal evidence for cures is there's no way of knowing how many people attempted the cure to no avail. We hear stories about people who tried it and had success.

I don't find the lack of controls an issue at this early stage of research. I presume the established cure rate is low enough that even one success can be considered statistically significant for such a small sample. If the purpose was to assess safety, not efficacy then small samples are appropriate because they limit the number of patients being exposed to the treatment until they know they aren't doing more harm than good with it.
 
Robinson, one reason why I find this sort of research more convincing than typical anecdotal evidence is that they know exactly how many people they attempted this treatment on. In the case of bee stings and other anecdotal evidence for cures is there's no way of knowing how many people attempted the cure to no avail. ....
That's a good point, Beth, in addition to the point one knows the hammer broke the window because it can be directly observed.
 

The full text of the study is here:
http://www.pnas.org/cgi/content/full/101/suppl_2/14631

(Bolding mine)

Only a small minority (10–20%) of melanoma patients vaccinated with tumor antigens such as MAGE-3.A1 have shown evidence of tumor regression. Because these vaccination trials have not included randomization with an untreated arm, one cannot rigorously exclude the possibility that the regressions observed are not due to the vaccine. Occasional spontaneous regressions of melanoma have been observed, but the frequency reported is at least 20 times lower than the frequency observed in the vaccination trials. The correlation between CTL responses and tumor regression observed in the ALVAC and dendritic cell trials supports the notion that the rejection is caused by the vaccine. But it does not rigorously prove it, because spontaneous regressions might result in the activation of new CTLs against the tumor.

See? They address the obvious point here. One you don't seem to grasp. Without isolating the procedure being done, or, as in this case, the vaccine, they can't really know. Which is why trials use placebos, blinding, large samples, all kinds of procedures to know what is really happening.
:i:
Just as you insist everybody must do, when you disagree with their conclusions.
 
That's a good point, Beth, in addition to the point one knows the hammer broke the window because it can be directly observed.

That is exactly the reasoning that some alternative health treatments use. Since you can do something, and you know exactly what it is, and you can observe what happens, you know that what you did led to what happened.

That you can do it over and over, and always get the same result, is proof that it works.
 
Robinson, one reason why I find this sort of research more convincing than typical anecdotal evidence is that they know exactly how many people they attempted this treatment on. .

I find it convincing because in the case of the one success, it was highly unlikely that the subject somehow boosted his immune system and had a spontaneous remission. So, because it was an unlikely event, it must be the treatment.


In the case of bee stings and other anecdotal evidence for cures is there's no way of knowing how many people attempted the cure to no avail. We hear stories about people who tried it and had success.

I don't know anything about bee stings and spontaneous remission.

I don't find the lack of controls an issue at this early stage of research. I presume the established cure rate is low enough that even one success can be considered statistically significant for such a small sample. If the purpose was to assess safety, not efficacy then small samples are appropriate because they limit the number of patients being exposed to the treatment until they know they aren't doing more harm than good with it.

Well, long term follow up on the one case is going to be required. If he gets cancer and dies anytime soon, the whole miracle thing is going to ring hollow.

All that being said, anything that can reduce or rid us of cancer, is a good thing. Miracle or not.
 
The full text of the study is here:
http://www.pnas.org/cgi/content/full/101/suppl_2/14631

(Bolding mine)

See? They address the obvious point here. One you don't seem to grasp. Without isolating the procedure being done, or, as in this case, the vaccine, they can't really know. Which is why trials use placebos, blinding, large samples, all kinds of procedures to know what is really happening.
:i:
Just as you insist everybody must do, when you disagree with their conclusions.
That is the wrong link, This one goes to the full article you've quoted.

The statement you quoted is not even close to what you posted. The statement, "one cannot rigorously exclude", is a far cry from what you said. So are you now revising your statement that the study in the OP had no more credibility than woo claims?

The researchers in your citation went on to explain what they meant by "cannot rigorously exclude" (emphasis mine):
the frequency [of spontaneous tumor regression] reported is at least 20 times lower than the frequency observed in the vaccination trials. The correlation between CTL responses and tumor regression observed in the ALVAC and dendritic cell trials supports the notion that the rejection is caused by the vaccine. But it does not rigorously prove it, because spontaneous regressions might result in the activation of new CTLs against the tumor.
Tumor regression 20 times more often with this type of treatment than spontaneous tumor remission is hardly akin to drawing a conclusion there is no more evidence here than woo.


Further, this is not the study I cited, nor were the comments specific to the study I cited.

Patient's own infection-fighting T cells put late-stage melanoma into long-term remission (again, emphasis mine).
Case is first to show safety and effectiveness of using cloned cells alone to kill tumors.

Yee and colleagues removed CD4+ T cells ... T cells specific to targeting the melanoma were then expanded vastly in the laboratory using modifications to existing methods. The lab-grown cells were then infused into the patient ... Two months later, PET and CT scans revealed no tumors. The patient remained disease free two years later, when he was last checked....

...Yee said. "For this patient we were successful, but we would need to confirm the effectiveness of therapy in a larger study."

Yee cautioned that these results, presented in the journal's "Brief Report" section, represent only one patient with a specific type of immune system whose tumor cells expressed a specific antigen. More studies are needed to confirm the effectiveness of the experimental T-cell therapy. If proven successful in more patients, Yee predicted this therapy could be used for the 25 percent of all late-stage melanoma patients who have the same immune-system type and tumor antigen....

...The patient received a dose of 5 billion cloned CD4+ T cells with specificity for the melanoma-associated NY-ESO-1 antigen. The cells persisted for at least 80 days in the patient's body. And, even though only 50 percent to 75 percent of the patient's tumor cells expressed the NY-ESO-1 antigen, the entire tumor regressed following the infusion. The scientists postulated that the patient's immune response was broadened to other antigens expressed by the tumor cells. Follow-up tests showed T-cell responses to two additional tumor antigens, MAGE-3 and MART-1.
You can easily misinterpret the wording here such as "More studies are needed to confirm the effectiveness of the experimental T-cell therapy". They are not saying more studies are needed to confirm it worked in this patient. They are saying more studies are needed to prove it will work in a broader number of patients.

Here is a previous study on this treatment. There has been a lot of work that preceded the study I cited in the OP.

Identification of CD4+ T Cell Epitopes from NY-ESO-1 Presented by HLA-DR Molecules
In this study, we describe the identification of MHC class II-restricted T cell epitopes from NY-ESO-1. Candidate CD4+ T cell peptides were first identified using HLA-DR4 transgenic mice immunized with the NY-ESO-1 protein. NY-ESO-1-specific CD4+ T cells were then generated from PBMC of a patient with melanoma stimulated with the candidate peptides in vitro. These CD4+ T cells recognized NY-ESO-1 peptides or protein pulsed on HLA-DR4+ EBV B cells, and also recognized tumor cells expressing HLA-DR4 and NY-ESO-1. A 10-mer peptide (VLLKEFTVSG) was recognized by CD4+ T cells.
Does that sound like they weren't sure about what they were doing or observing because they didn't have a control group?
 
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That is exactly the reasoning that some alternative health treatments use. Since you can do something, and you know exactly what it is, and you can observe what happens, you know that what you did led to what happened.

That you can do it over and over, and always get the same result, is proof that it works.
So how many windows do you need to break with a hammer to be sure a hammer swung into glass is the cause of the glass breaking?
 
I find it convincing because in the case of the one success, it was highly unlikely that the subject somehow boosted his immune system and had a spontaneous remission. So, because it was an unlikely event, it must be the treatment. ....
So "5 billion cloned CD4+ T cells with specificity for the melanoma-associated NY-ESO-1 antigen" infused into a patient where "50 percent to 75 percent of the patient's tumor cells expressed the NY-ESO-1 antigen" is irrelevant and according to you, all that we can really go by here when drawing our conclusion is the rarity of spontaneous tumor regression.

Is that your position?
 

I'm not quite sure what is going on with the links, or why you are confused.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=521999 I never saw before.

This is the link you posted, which I quoted from your post.
http://www.pnas.org/cgi/content/abstract/101/suppl_2/14631

This is the full text, from that link.
http://www.pnas.org/cgi/content/full/101/suppl_2/14631

Note the number of the file, 14631
It seems to be the same paper that you linked to
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=521999

So I don't understand how you can say it is the wrong link. I quoted from the paper at the link I used in my post. Get a grip there.
 

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